Diabetes-induced osteopathy represents a clinically significant but under recognised complication of both type 1 and type 2 diabetes, characterised by increased fracture risk despite normal or modestly reduced bone mineral density. This paradox reflects deterioration in bone quality driven by advanced glycation end products, oxidative stress, chronic inflammation, impaired osteoblast function, enhanced osteoclast activity and disrupted osteocyte signalling. Although experimental models have provided valuable mechanistic insights, current chemically induced, diet-induced, and genetic systems each reproduce only selective aspects of the human disease. Most models prioritise metabolic validation, particularly hyperglycaemia, while skeletal endpoints are often secondary and incompletely characterised. Moreover, reductions in bone mineral density do not consistently correlate with microarchitectural or biomechanical deficits. A mechanism-oriented framework that integrates metabolic, structural, molecular, and biomechanical assessments may better capture disease complexity. Refining experimental design and endpoint standardisation could enhance translational relevance and support the development of therapeutic strategies targeting bone fragility beyond glycaemic control.
Qamar et al. (Mon,) studied this question.